Explore the vast range of titles available.

Transpacific Cartographies examines how contemporary Chinese diasporic narratives address the existential loss of home for immigrant communities at a time of global precarity and amid rising Sino-US tensions. Focusing on cultural productions of the Chinese diaspora from the 1990s to the present -- including novels by the Sinophone writers Yan Geling (The Criminal Lu Yanshi), Shi Yu (New York Lover), Chen Qian (Listen to the Caged Bird Sing), and Rong Rong (Notes of a Couple), as well as by the Anglophone writer Ha Jin (A Free Life; A Map of Betrayal), selected TV shows (Beijinger in New York; The Way We Were), and online literature -- Melody Yunzi Li argues that the characters in these stories create multilayered maps that transcend the territorial boundaries that make finding a home in a foreign land a seemingly impossible task. In doing so, these \"maps\" outline a transpacific landscape that reflects the psycho-geography of homemaking for diasporic communities. Intersecting with and bridging Sinophone studies, Chinese American studies, and diaspora studies and drawing on theories of literary cartography, Transpacific Cartographies demonstrates how these \"maps\" offer their readers different paths for finding a sense of home no matter where they are.  

Background Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive treatment for ischemic stroke. Astrocytes regulation has been suggested as one mechanism for rTMS effectiveness. But how rTMS regulates astrocytes remains largely undetermined. There were neurotoxic and neuroprotective phenotypes of astrocytes (also denoted as classically and alternatively activated astrocytes or A1 and A2 astrocytes) pertaining to pro- or anti-inflammatory gene expression. Pro-inflammatory or neurotoxic polarized astrocytes were induced during cerebral ischemic stroke. The present study aimed to investigate the effects of rTMS on astrocytic polarization during cerebral ischemic/reperfusion injury. Methods Three rTMS protocols were applied to primary astrocytes under normal and oxygen-glucose deprivation/reoxygenation (OGD/R) conditions. Cell survival, proliferation, and phenotypic changes were assessed after 2-day treatment. Astrocytes culture medium (ACM) from control, OGD/R, and OGD/R + rTMS groups were mixed with neuronal medium to culture neurons for 48 h and 7 days, in order to explore the influence on neuronal survival and synaptic plasticity. In vivo, rats were subjected to middle cerebral artery occlusion (MCAO), and received posterior orbital intravenous injection of ACM collected from different groups at reperfusion, and at 3 days post reperfusion. The apoptosis in the ischemic penumbra, infarct volumes, and the modified Neurological Severity Score (mNSS) were evaluated at 1 week after reperfusion, and cognitive functions were evaluated using the Morris Water Maze (MWM) tests. Finally, the 10 Hz rTMS was directly applied to MCAO rats to verify the rTMS effects on astrocytic polarization. Results Among these three frequencies, the 10 Hz protocol exerted the greatest potential to modulate astrocytic polarization after OGD/R injury. Classically activated and A1 markers were significantly inhibited by rTMS treatment. In OGD/R model, the concentration of pro-inflammatory mediator TNF-α decreased from 57.7 to 23.0 рg/mL, while anti-inflammatory mediator IL-10 increased from 99.0 to 555.1 рg/mL in the ACM after rTMS treatment. The ACM collected from rTMS-treated astrocytes significantly alleviated neuronal apoptosis induced by OGD/R injury, and promoted neuronal plasticity. In MCAO rat model, the ACM collected from rTMS treatment decreased neuronal apoptosis and infarct volumes, and improved cognitive functions. The neurotoxic astrocytes were simultaneously inhibited after rTMS treatment. Conclusion Inhibition of neurotoxic astrocytic polarization is a potential mechanism for the effectiveness of high-frequency rTMS in cerebral ischemic stroke.

Oligovascular coupling contributes to white matter vascular homeostasis. However, little is known about the effects of oligovascular interaction on oligodendrocyte precursor cell (OPC) changes in chronic cerebral ischemia. Here, using a mouse of bilateral carotid artery stenosis, we show a gradual accumulation of OPCs on vasculature with impaired oligodendrogenesis. Mechanistically, chronic ischemia induces a substantial loss of endothelial caveolin-1 (Cav-1), leading to vascular secretion of heat shock protein 90α (HSP90α). Endothelial-specific over-expression of Cav-1 or genetic knockdown of vascular HSP90α restores normal vascular-OPC interaction, promotes oligodendrogenesis and attenuates ischemic myelin damage. miR-3074(−1)−3p is identified as a direct inducer of Cav-1 reduction in mice and humans. Endothelial uptake of nanoparticle-antagomir improves myelin damage and cognitive deficits dependent on Cav-1. In summary, our findings demonstrate that vascular abnormality may compromise oligodendrogenesis and myelin regeneration through endothelial Cav-1, which may provide an intercellular mechanism in ischemic demyelination. OPC-vascular coupling contributes to myelin maintenance. Here the authors show Cav-1 stabilizes interactions and mediates OPC maturation in ischemia.

BackgroundDespite the use of lipid-lowering and anti-inflammatory treatments, the progression of atherosclerosis is relentless in most patients. This suggests the presence of in situ pathological factors that continuously exacerbate lesions. We hypothesized that extracellular vesicles (EVs) within the atherosclerotic microenvironment might act as in situ stimulatory factors on vascular smooth muscle cells (VSMCs), thereby exacerbating atherosclerosis.Methods and resultsA local atherosclerosis model was induced using Ldlr knockout (Ldlr KO) rats fed a high-cholesterol diet and subjected to partial carotid ligation. Immunofluorescence, Western blot (WB), and single-cell sequencing confirmed the phenotypic switching of VSMCs in atherosclerotic plaques from both rats and humans. The phenotypic switching of VSMCs in atherosclerotic rats was characterized by reduced expression of VSMC contraction markers and increased expression of LGALS3, PDGFRB, and SCA1. GW4869 inhibited the phenotypic switching of VSMCs in atherosclerotic plaques in a rat model. EVs were extracted from atherosclerotic carotid tissues using differential centrifugation. Chitosan thermosensitive hydrogels were used for in situ delivery of EVs into the arterial wall of the carotid artery. Immunofluorescence staining revealed that atherosclerotic plaque-derived EVs (AS-EVs) promoted VSMC phenotypic switching and downregulated the expression of VSMC contractile markers in vitro. miRNA analysis of EVs derived from atherosclerotic plaques of rats identified miR-23a-3p and its target gene Myl12b. To investigate the underlying mechanisms, engineered EVs loaded with miR-23a-3p were used to mimic AS-EVs. AS-EVs potentially regulate MRTFA nuclear translocation via miR-23a-3p/Myl12b, inhibit contractile marker expression, promote VSMC phenotypic switching, and further promote carotid artery remodelling.ConclusionWe conclude that AS-EVs promote VSMC phenotypic switching and exacerbate atherosclerosis.

Numerical methods, such as finite element or finite difference, have been widely used in the past decades for modeling solid mechanics problems by solving partial differential equations (PDEs). Differently from the traditional computational paradigm employed in numerical methods, physics-informed deep learning approximates the physics domains using a neural network and embeds physics laws to regularize the network. In this work, a physics-informed neural network (PINN) is extended for application to linear elasticity problems that arise in modeling non-uniform deformation for a typical open-holed plate specimen. The main focus will be on investigating the performance of a conventional PINN approach to modeling non-uniform deformation with high stress concentration in relation to solid mechanics involving forward and inverse problems. Compared to the conventional finite element method, our results show the promise of using PINN in modeling the non-uniform deformation of materials with the occurrence of both forward and inverse problems.

Introduction: Neutrophil extracellular traps play a role in the pathophysiology of stroke and are associated with severity and mortality. We aimed to investigate whether the citrullinated histone H3 (CitH3), a biomarker for neutrophil extracellular traps formation, is associated with the white matter lesion (WML) burden in ischemic stroke patients. Methods: Between September 2021 and April 2022, 322 patients were enrolled in this prospective observational cohort study. Serum CitH3 levels were measured after admission using an enzyme-linked immunosorbent assay. WMLs severity was graded according to the Fazekas scale and conceptually defined as mild (total Fazekas score 0–2) and severe (total Fazekas score 3–6). We used multivariable regression models to determine the relationship between CitH3 concentrations and the severity of WMLs burden. Results: One-hundred and forty-eight (46.0%) patients were diagnosed with severe WMLs burden after admission. Increased CitH3 levels (first quartile vs. fourth quartile of H3Cit, odds ratio, 3.311, 95% confidence interval, 1.336–8.027; p = 0.011) were independently associated with a greater WML burden in the fully adjusted multivariable model. Similar results were found when the H3Cit was analyzed as a continuous variable. Furthermore, the multiple-adjusted spline regression model showed a linear association between H3Cit levels and severe WMLs (P = 0.001 for linearity). Conclusions: In the present study, increased CitH3 levels were positively associated with extensive WMLs in ischemic stroke patients, indicating a role of neutrophil extracellular traps formation in the pathogenesis of WMLs.

Nightclubs flourished in San Francisco’s Chinatown in the late 1930s when it became a nightlife destination. To Chinese Americans, however, San Francisco nightclubs became a new site at the time for them to re-explore their identities. For some, visiting these nightclubs became a way for them to escape from traditional Chinese values. For others, it became a way to satisfy Western stereotypes of Chinese culture. Lisa See’s China Dolls (2015) describes three young oriental women from various backgrounds that become dancers at the popular Forbidden City nightclub in San Francisco in the late 1930s. Through the three girls’ precarious careers and personal conflicts, Lisa See proposes the San Francisco nightclub as both a site for them to articulate their new identities beyond their restricted spheres and a site for them to perform the expected stereotypical Asian images from Western perspectives. It was, at that time, a struggle for the emergence of modern Chinese women but particularly a paradox for Chinese-American women. The space of the Chinese-American nightclub, which is exotic, erotic, but stereotypical, represents contradictions in the Chinese-American identity. Through studying Lisa See’s novel along with other autobiographies of the Chinese American dancing girls, I argue that San Francisco nightclubs, as represented in Lisa See’s novel, embody the paradox of Chinese American identities as shown in the outfits of Chinese American chorus girls—modest cheongsams outside and sexy, burlesque costumes underneath.

A weighted fracturing fluid with superlow guar gum concentration was developed by synthesizing a polyboric acid cross-linker. The density of this fluid is 1.365 g/cm3 and can withstand very high temperature up to 175°C. In this study, a weighting agent was selected, and crosslinking ligands and boric acid were optimized. The crosslinking performance, base fluid viscosity, rheology, and gel-breaking performance of this fracturing fluid were studied. Compared with the conventional weighted fracturing fluid, the concentration of guar gum in the new weighted fracturing fluid can be reduced by 30% at the same temperature condition; moreover, crosslinking can be delayed by 2 minutes. The concentration of gel breaker used in this fluid can be significantly reduced to 0.005%∼0.01%. Two field tests were conducted in Jidong oil field, and both of them achieved great success.

International students are a bridge between Chinese and foreign cultures, but they still face multiple dilemmas in Chinese cultural communication due to different cultural backgrounds and values. In this paper, we utilize the subsumption sorting algorithm to sort the amount of cultural communication of international students’ exchanges, which is dynamically switched by a combination of two methods: back-block forward interpolation and header exchange. The D-S monopolistic competition model is used to construct the theoretical model of international student exchange that affects China’s international cultural communication power. The CES utility function is used to construct China’s international cultural communication network, which calculates the total amount of communication culture of cross-cultural exchanges between international students. In the end, an analysis of 85 international student samples revealed a correlation between international student exchanges and China’s international cultural communication. The results show that the correlation coefficient between international student exchanges and China’s international cultural communication is 0.305 > 0.05, indicating that international student exchanges have a positive promotion effect on China’s international cultural communication. This study examines the general law of international cultural communication, which is crucial in promoting Chinese culture worldwide.

Neuroinflammation is initiated in response to ischemic stroke, generally with the hallmarks of microglial activation and collateral brain injury contributed by robust inflammatory effects. Triggering receptor expressed on myeloid cells (TREM)-1, an amplifier of the innate immune response, is a critical regulator of inflammation. This study identified that microglial TREM-1 expression was upregulated following cerebral ischemic injury. After pharmacologic inhibition of TREM-1 with synthetic peptide LP17, ischemia-induced infarction and neuronal injury were substantially alleviated. Moreover, blockade of TREM-1 can potentiate cellular proliferation and synaptic plasticity in hippocampus, resulting in long-term functional improvement. Microglial M1 polarization and neutrophil recruitment were remarkably abrogated as mRNA levels of M1 markers, chemokines, and protein levels of myeloperoxidase and intracellular adhesion molecule-1 (ICAM-1) were decreased by LP17. Mechanistically, both in vivo and in vitro, we delineated that TREM-1 can activate downstream pro-inflammatory pathways, CARD9/NF-κB, and NLRP3/caspase-1, through interacting with spleen tyrosine kinase (SYK). In addition, TREM-1-induced SYK initiation was responsible for microglial pyroptosis by elevating levels of gasdermin D (GSDMD), N-terminal fragment of GSDMD (GSDMD-N), and forming GSDMD pores, which can facilitate the release of intracellular inflammatory factors, in microglia. In summary, microglial TREM-1 receptor yielded post-stroke neuroinflammatory damage via associating with SYK.